Regulation of transcription factor suppresses malignant properties of cancer cells with changes in glycosylation
| Project/Area Number |
23590070
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Nagaoka University of Technology |
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Principal Investigator |
SATO Takeshi 長岡技術科学大学, 工学部, 准教授 (30291131)
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| Co-Investigator(Kenkyū-buntansha) |
FURUKAWA Kiyoshi 長岡技術科学大学, 工学部, 教授 (10190133)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | 転写因子 / がん / 悪性形質 / 腫瘍形成 / 細胞運動 / 糖鎖 / 糖タンパク質 / シグナル伝達 |
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| Research Abstract |
In this grant, we established the Sp1-knockdown cells from A549 human lung carcinoma cells by RNAi technique, and examined the relationship between protein glycosylation and malignant properties. Lectin blot analysis showed that decreased galactosylation of N-glycans is observed for E-cadherin in the Sp1-knockdown cells. The gene expression level of beta-1,4-GalT I decreased significantly by knockdown of Sp1. Analysis of the promoter region of the human beta-1,4-GalT I gene revealed that the Sp1-binding site are critical for the expression of the gene. Moreover, knockdown of Sp1 resulted in suppression of the tumorigenic potential and migratory activity of A549 cells. Furthermore, the EGF receptor signaling was reduced by knockdown of Sp1. The study indicates that the malignant properties of cancer cells can be suppressed by regulating Sp1 through changes in protein glycosylation, and suggests that Sp1 may be a potential target for cancer therapy.
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Report
(4 results)
Research Products
(32 results)
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[Journal Article] Enhanced ex- pression of theβ4-galactosyltrans- ferase 2 gene impairs mammalian tumor growth2014
Author(s)
Tagawa, M., Shirane, K., Yu, L., Sato, T., Furukawa, S., Mizuguchi, H., Kuji, R., Kawamura, K., Takahashi, N., Kato, K., Hayakawa, S., Sawada, S., and Furukawa, K
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Journal Title
Cancer Gene Ther
Volume: (in press)
Related Report
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[Journal Article] Gene expression levels ofβ4-galac- tosyltransferase 5 correlate with the tumorigenic potentials of B16-F10 mouse melanoma cells2014
Author(s)
Shirane, K., Kuji, R., Tareyanagi, C., Sato, T., Kobayashi, Y., Furukawa, S., Murata, T., Kubota, S., Ishikawa, Y., Segawa, K., and Furukawa, K
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Journal Title
Glycobiology
Volume: 24 (6)
Pages: 532-541
Related Report
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[Journal Article] Gene expression levels of β-1,4-galactosyltransferase V correlate with the tumorigenic potentials of B16-F10 mouse melanoma cells2014
Author(s)
Shirane, K., Kuji, R., Tareyanagi, C., Sato, T., Kobayashi, Y., Furukawa, S., Murata, T., Kubota, S., Ishikawa, Y., Segawa, K., and Furukawa, K.
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Journal Title
Glycobiology
Volume: 24
Pages: 532-541
Related Report
Peer Reviewed
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[Journal Article] Enhanced expression of the β4-galactosyltransferase 2 gene impairs mammalian tumor growth2014
Author(s)
Tagawa, M., Shirane, K., Yu, L., Sato, T., Furukawa, S., Mizuguchi, H., Kuji, R., Kawamura, K., Takahashi, N., Kato, K., Hayakawa, S., Sawada, S., and Furukawa, K.
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Journal Title
Cancer Gene Therapy
Volume: 21
Related Report
Peer Reviewed
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[Book] UDP-Gal :β-N-Acetylgluco- samineβ4-Galactosyltransferases (β4GalT2,β4GalT3, andβ4GalT4), UDP-Gal : Glucosylceramideβ4-Galac- tosyltransferases (β4GalT5 andβ4GalT6), and UDP-Gal : Xylosylproteinβ4-Galactosyltransferase (β4GalT7, galactosyltransferase I) in Handbook of Glycosyltransferase and Related Genes2014
Author(s)
Furukawa, K., Clausen, H., and Sato, T (Taniguchi, N. et al. eds)
Publisher
Springer(in press)
Related Report
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